Abstract: PO1746
Thrombotic Microangiopathy and AKI Induced After Intravitreal Injection of Vascular Endothelial Growth Factor Inhibitors
Session Information
- Glomerular Diseases: Vasculitis and TMA
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1202 Glomerular Diseases: Immunology and Inflammation
Authors
- Hanna, Ramy Magdy, University of California Irvine, Orange, California, United States
- Patel, Sapna Singh, Long Beach Medical Center, Long Beach, California, United States
- Tran, Ngoc Gia, Long Beach Medical Center, Long Beach, California, United States
- Jhaveri, Kenar D., Northwell Health, Great Neck, New York, United States
- Kalantar-Zadeh, Kamyar, University of California Los Angeles, Los Angeles, California, United States
- Kurtz, Ira, University of California Los Angeles, Los Angeles, California, United States
Introduction
Vascular Endothelial Growth Factor (VEGF) inhibition can cause worsening hypertension, proteinuria, acute and chronic kidney injury, as well as glomerular disease from Thrombotic Microangiopathy (TMA) and other nephrotic disorders when given systemically. These same agents are given intravitreally for age related macular degeneration (AMD) and Diabetic Retinopathy (DR) among other ophthalmologic conditions, albeit at lower doses than those given for systemic indications. Systemic absorption of anti-VEGF agents when given intravitreally has been shown consistently along with evidence of significant intravascular VEGF suppression. While worsening hypertension has only been seen in some large-scale studies, case reports show worsening proteinuria and diverse glomerular diseases. These include TMA-associated lesions like Focal and Segmental Glomerulosclerosis with Collapsing Features (cFSGS).
Case Description
In this paper, we report 3 cases of TMA likely associated with use of intravitreal anti VEGF therapy. These patients developed the signature lesion of VEGF blockade in a 6 month – 11-month time frame after starting intravitreal VEGF inhibitors.
Discussion
The literature is reviewed showing similar cases. Intravitreal VEGF blockade may cause these adverse events in a hitherto unidentified subgroup of patients. Further studies are needed to determine the event rate and identify which patients are at increased risk for hypertension, proteinuria worsening, renal injury, and glomerular diseases from intravitreal VEGF blockade.